Angiotensin, ACE-inhibitors and endothelial control of vasomotor tone. | Semantic Scholar (2024)

In conditions involving progressive dysfunction of the endothelium, vascular deposition of platelets increases the local levels of platelet-derived growth factor, and the antiproliferative effects of calcium antagonists may thus be particularly important.

Maximum information related to ACE inhibitors, hypertension and atherosclerosis has been compiled for the benefit of physicians and patients.

RAS antagonist pharmacology may help to understand the hemodynamic risk of anesthesia in RAS-blocked patients, to identify predisposing factors, and to determine the potential benefit of RAS antagonists during anesthesia and surgery.

Results reveal that ET activates the plasmatic coagulation system and induces an ARF accompanied by impairment of pulmonary function, indicating a consumptive coagulopathy.

Polymorphisms in genes coding for the renin-angiotensin system seem associated with hypertension and left ventricular hypertrophy, and these observations may be clinically relevant as inhibition of local renIn-angiotsin systems may be an important prerequisite to obtain an optimal clinical effect.

Hormonal products of the vascular endothelium may provide the final common pathway for vessel autoregulation in response to varying physiologic stress in many vascular beds, including the retina and choroid.

A number of independent and complementary mechanisms pointing to a role of ACE and ACE inhibition in coronary artery disease are summarized.

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It is speculated that ACE inhibitors improve endothelial function in SHRs not by inhibiting the synthesis of PGH2 but by increasing the release or the action of endothelium-derived relaxing factor.

Evidence is provided that the renin-angiotensin system is important in acute blood pressure regulation during sodium depletion, anesthesia, and hemorrhage, as well as in the initiation of renovascular hypertension and in the development of the syndrome of congestive heart failure.

Vascular endothelin production in hypertension remains controversial but appears mostly normal; it is augmented in the presence of vascular disease or renal insufficiency and the reactivity of vascular smooth muscle may be normal, increased, or reduced.

ACE inhibitors potentiate endothelium-dependent relaxations to submaximal concentrations of bradykinin in bovine and human coronary arteries and this local mechanism occurs regardless of elevated bradyKinin concentrations in the blood and reduced angiotensin II generation.

Results suggest that converting enzyme is indeed a powerful modulator of bradykinin action and that other enzymatic pathways of bradaykinin metabolism present in the vascular wall could mask its action.

To study whether low concentrations of endothelin-1 potentiate the effects of other vasoconstrictor hormones, suspended isolated human internal mammary and left anterior descending coronary artery rings in organ chambers for isometric tension recording.

Chronic blockade of the renin-angiotensin system or voltage-operated calcium channels reduces BP and improves endothelial dysfunction in the resistance circulation of SHR and may contribute to normalization of peripheral vascular resistance during antihypertensive treatment.

Angiotensin II stimulates the endothelial production of endothelin in situ and therapy potentiates contractions to norepinephrine in mesenteric resistance arteries of spontaneously hypertensive rats, suggesting that vascular endothelins production acts as an amplifier of the pressor effects of the renin-angiotens in system that may play an important role in hypertension.

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